Transcriptome analysis reveals the underlying mechanism of heptanal against Aspergillus flavus spore germination
Sheng-Fa Li1,2, Shuai-Bing Zhang3,4, Yang-Yong Lv1,2
1College of Biological Engineering, Henan University of Technology, 100 Lianhua Street, Zhengzhou, Henan, 450001, People's Republic of China.
Abstract:
Methods of controlling Aspergillus flavus contamination in agro-products have attracted attention because of its impact on global food security. We previously reported that the natural cereal volatile heptanal could effectively inhibit A. flavus growth and showed great potential as a bio-preservative agent. In this study, the minimum inhibitory concentration and minimum fungicide concentration of heptanal could change the surface morphology of A. flavus spores, causing them to wrinkle and collapse. Transcriptomic analysis showed that heptanal treatment significantly changed the expression of several genes involved in cell wall and plasma damage, reactive oxygen species (ROS) accumulation, energy metabolism, AMPK-activated protein kinase, biosynthesis of unsaturated fatty acids, RNA degradation, and DNA replication. Heptanal-induced early apoptosis of A. flavus spores was characterized by decreased mitochondrial membrane potential, increased intracellular ROS production, and DNA fragmentation. This study provides new insight into the inhibitory mechanism of heptanal against A. flavus and points to its potential application as a bio-preservative. KEY POINTS: • Heptanal can effectively inhibit A. flavus growth in cereal grains. • The transcriptional changes in A. flavus spores exposed to heptanal were analyzed. • The antifungal mechanism of heptanal against A. flavus was elucidated.
More Related Videos
10:01Quantification of Fungal Colonization, Sporogenesis, and Production of Mycotoxins Using Kernel Bioassays
Published on: April 23, 2012
09:44RNAi-mediated Control of Aflatoxins in Peanut: Method to Analyze Mycotoxin Production and Transgene Expression in the Peanut/Aspergillus Pathosystem
Published on: December 21, 2015
